ReviewGeroScience2026
A two-step model of age-associated autoreactivity: B cell-intrinsic aging meets inflammaging.
Review in GeroScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is associated with declining protective immunity and increased autoreactivity, yet the mechanisms linking these processes remain incompletely understood. B lymphocytes are central to this paradox because they integrate antigen recognition, innate signaling, and differentiation under tightly regulated tolerance checkpoints. This review advances the hypothesis that aging appears to drive a progressive, B cell-intrinsic relaxation of central and peripheral tolerance, leading to the accumulation of autoreactive clones. These defects are reinforced by transcriptional, epigenetic, metabolic, and signaling remodeling that durably reshapes B-cell responsiveness. In parallel, chronic low-grade inflammation (inflammaging) acts as a selective pressure that preferentially expands inflammation-adapted B-cell subsets, including age-associated B cells (ABCs) and related DN2 populations, rather than uniformly activating the B-cell compartment. This synergy promotes extrafollicular differentiation while bypassing key germinal-center tolerance checkpoints, thereby enriching for autoreactive B-cell states. A unifying model is proposed in which intrinsic aging establishes susceptibility, whereas inflammaging amplifies pathogenic B-cell programs, linking immune senescence to autoimmunity and highlighting potential targets for selective therapeutic intervention.
Indexed as
Identifiers
42768164What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.